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Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation
Published on: August 23, 2018
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Myeloma-Modified Adipocytes Exhibit Metabolic Dysfunction and a Senescence-Associated Secretory Phenotype
Heather Fairfield1,2,3, Amel Dudakovic4, Casper M Khatib5
1Maine Medical Center Research Institute, Scarborough, Maine.
Cancer Research
|November 21, 2020
Summary
Multiple myeloma cells interact with bone marrow adipocytes, causing changes that promote cancer growth and drug resistance. Targeting adipocyte senescence may offer new therapeutic strategies for multiple myeloma.
Area of Science:
- Oncology
- Cell Biology
- Metabolic Diseases
Background:
- Bone marrow adipocytes (BMAd) and bone marrow adipose tissue (BMAT) are increasingly recognized for their role in cancer progression.
- BMAT expansion with aging and obesity correlates with multiple myeloma prevalence, suggesting a link between adipocytes and myeloma.
- Reciprocal interactions between myeloma cells and BMAd may significantly influence multiple myeloma pathogenesis and treatment outcomes.
Purpose of the Study:
- To investigate the bidirectional interactions between multiple myeloma cells and bone marrow adipocytes.
- To determine the role of these interactions in multiple myeloma development and response to therapy.
- To explore potential therapeutic strategies targeting these interactions.
Main Methods:
- Analysis of bone marrow biopsies from multiple myeloma patients before and after treatment.
- Preclinical murine models of multiple myeloma.
- In vitro co-culture systems of myeloma cells and adipocytes.
- Assessment of adipocyte gene expression, cytokine secretion, and senescence markers.
- Evaluation of myeloma cell resistance to chemotherapy.
Main Results:
- Multiple myeloma patients showed reduced BMAT, which was restored post-treatment.
- Myeloma cells decreased BMAT in preclinical models and in vitro co-cultures.
- Myeloma cells induced metabolic and gene expression changes in adipocytes, leading to a senescent-like phenotype.
- Bone marrow adipocytes conferred resistance to dexamethasone-induced apoptosis and cell-cycle arrest in myeloma cells.
- Senescence markers were elevated in the bone marrow of tumor-bearing mice.
Conclusions:
- Bidirectional communication between myeloma cells and BMAd is crucial in multiple myeloma pathogenesis.
- Myeloma cells induce senescence and metabolic alterations in adipocytes, potentially driving drug resistance.
- Targeting adipocyte senescence presents a novel therapeutic avenue for multiple myeloma treatment.
- This study reframes the understanding of cancer cell interactions within the bone marrow microenvironment.
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